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细胞内铜/锌超氧化物歧化酶在人胸主动脉夹层的表达研究 被引量:2

Expression of intracellular copper zinc superoxide dismutase in human thoracic aortic dissection
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摘要 目的:探讨细胞内铜/锌超氧化物岐化酶(copper zinc superoxide dismutase,Cu/Zn-SOD,SOD-1)在人胸主动脉夹层(humanthoracic aortic dissection,hTAD)中的表达情况及其在hTAD中的可能作用。方法:蛋白质印迹法(Western blot,WB)检测SOD-1在TAD和正常人胸主动脉(NA)中膜组织中的表达情况,免疫组织化学染色(immunohistochemistry,IHC)验证SOD-1在动脉壁中的表达和定位。结果:蛋白质印迹和免疫组化染色均显示SOD-1在TAD组表达量较NA组减低(P<0.05);免疫组化染色进一步显示,SOD-1主要位于主动脉壁中膜平滑肌细胞的胞质内,其在夹层主动脉壁中膜撕开处表达缺失。结论:SOD-1在TAD中表达量减少,可能由于参与氧化应激引起的脂质过氧化和炎症反应,以及细胞外基质(extracellular matrix,ECM)的降解等机制所致。 Objective:To investigate the intracellular copper zinc superoxide dismutase (SOD-1) expression in human thoracic aortic dissection (hTAD) and its possible roles in TAD.Methods:Western blot was performed to detect the expression of SOD-1 in dissected thoracic aortas and normal controls.Immunohistochemistry was used to validate its expression and localization. Results: Western blot and immunohistochemistry showed that the SOD-1 expression decreased in TAD compared with normaI controls (P 〈0.05).Immunohistochemistry showed further that SOD-1 mainly Iocalized in the cytoplasm of smooth muscle cells (SMCs) in the media, disappeared in the edges of the region where the media was divulsed.Conclusion:The SOD-1 expression decreased in TAD, which could attribute to some mechanisms such as participating the lipid peroxidation and Inflammatory reaction induced by oxidative stress, in addition,the degradation of extracellular matrix(ECM).
出处 《现代生物医学进展》 CAS 2010年第3期421-424,共4页 Progress in Modern Biomedicine
基金 国家自然科学基金(30600599) 上海市科委基础重点项目(08JC1406100)
关键词 细胞内铜/锌超氧化物岐化酶(SOD-1) 胸主动脉夹层(TAD) 氧化应激 脂质过氧化 细胞外基质 Copper zinc superoxide dismutase (SOD-1) Thoracic aortic dissection (TAD) oxidative stress lipid peroxidation extracellular matrix(ECM)
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